Insulin is released just by the sight and smell of a meal, but now, researchers report in Cell Metabolism that this insulin release depends on a short-term inflammatory response that takes place in these circumstances. In overweight individuals, however, this inflammatory response is so excessive that it can impair insulin secretion.
Even the anticipation of a forthcoming meal triggers a series of responses in the body. Insulin is released in this neurally mediated (or cephalic) phase of insulin secretion.
Meal stimulates immune defence
Until now, it was unclear how the sensory perception of a meal generated a signal to the pancreas to ramp up insulin production. Now, researchers from the University of Basel and University Hospital Basel have identified an important piece of the puzzle: an inflammatory factor known as interleukin 1 beta (IL1B), which is also involved in the immune response to pathogens or in tissue damage.
“The fact that this inflammatory factor is responsible for a considerable proportion of normal insulin secretion in healthy individuals is surprising, because it’s also involved in the development of type 2 diabetes,” explained study leader Professor Marc Donath from the Department of Biomedicine and the Clinic of Endocrinology.
Chronic inflammation damaging the insulin-producing cells of the pancreas is one of the causes of type 2 diabetes. This is another situation in which IL1B plays a key role – in this case, it is produced and secreted in excessively large quantities. Thus, researchers are investigating whether inhibiting IL1B could be a treatment for diabetes.
Short-lived inflammatory response
Circumstances are different when it comes to neurally mediated insulin secretion: “The smell and sight of a meal stimulate specific immune cells in the brain known as the microglia,” said study author Dr Sophia Wiedemann, resident physician for internal medicine. “These cells briefly secrete IL1B, which in turn affects the autonomic nervous system via the vagus nerve.” This system then relays the signal to the pancreas.
In the case of morbid obesity, however, this neurally mediated phase of insulin secretion is disrupted. Specifically, by the initial excessive inflammatory response, as explained by doctoral candidate Kelly Trimigliozzi, who carried out the main part of the study in collaboration with Dr Wiedemann.
“Our results indicate that IL1B plays an important role in linking up sensory information such as the sight and smell of a meal with subsequent neurally mediated insulin secretion – and in regulating this connection,” Prof Marc Donath said.
Source: EurekAlert!
